Evidence map›Paper›PMID 16421294›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006

Reversal of neuronal migration in a mouse model of fetal alcohol syndrome by controlling second-messenger signalings.

Tatsuro Kumada, Madepalli K Lakshmana, Hitoshi Komuro

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
10.3field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. The Role of Galanin in Cerebellar Granule Cell Migration in the Early Postnatal Mouse during Normal Development and after Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Prenatal Environment That Affects Neuronal Migration.Frontiers in cell and developmental biology · 2019
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Control of cortical neuronal migration by glutamate and GABA.Frontiers in cellular neuroscience · 2015
    Review
  15. Cellular commitment in the developing cerebellum.Frontiers in cellular neuroscience · 2014
    Review
  16. Article
  17. Rescue of neuronal migration deficits in a mouse model of fetal Minamata disease by increasing neuronal Ca2+ spike frequency.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  18. Article
  19. Article
  20. Myelination and axonal electrical activity modulate the distribution and motility of mitochondria at CNS nodes of Ranvier.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Tatsuro KumadaDepartment of Neurosciences, Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Madepalli K Lakshmana
Hitoshi Komuro
Cleveland Clinic · US

Funding

Effects of alcohol on neuronal cell migrationR01AA013613 · NIAAA · CLEVELAND CLINIC LERNER COL/MED-CWRU · PI KOMURO, HITOSHI · 2002 to 2005
$1.1M
NIAAA NIH HHS AA 13613NIAAA NIH HHS R01 AA013613
6 · The paper itself

Abstract

The brains of fetal alcohol syndrome patients exhibit impaired neuronal migration, but little is known about the mechanisms underlying this abnormality. Here we show that Ca2+ signaling and cyclic nucleotide signaling are the central targets of alcohol action in neuronal cell migration. Acute administration of ethanol reduced the frequency of transient Ca2+ elevations in migrating neurons and cGMP levels and increased cAMP levels. Experimental manipulations of these second-messenger pathways, through stimulating Ca2+ and cGMP signaling or inhibiting cAMP signaling, completely reversed the action of ethanol on neuronal migration in vitro as well as in vivo. Each second messenger has multiple but distinct downstream targets, including Ca2+/calmodulin-dependent protein kinase II, calcineurin, protein phosphatase 1, Rho GTPase, mitogen-activated protein kinase, and phosphoinositide 3-kinase. These results demonstrate that the aberrant migration of immature neurons in the fetal brain caused by maternal alcohol consumption may be corrected by controlling the activity of these second-messenger pathways.

Indexed as

Cell Migration InhibitionDisease Models, AnimalAnimalsAnimals, NewbornCaffeineCells, CulturedCerebellumDose-Response Relationship, DrugEthanolFemaleFetal Alcohol Spectrum DisordersMiceNeuronsN-MethylaspartatePregnancySecond Messenger SystemsCaffeineEthanolN-Methylaspartate

Identifiers

PMID16421294
PMCPMC6675380
OpenAlexW2127705828

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.